Continuous twitching of a part of the body or face
Introduction
Introduction Limited convulsions: twitching for a local part of the body or face. For example, localized sports epilepsy often manifests as repeated convulsions of the mouth, eyelids, hands or feet; if the convulsion starts from one place, it gradually expands according to the arrangement of the cerebral cortex movement area, that is, from the side of the thumb, the extension and the wrist , arms, shoulders, is Jackson epilepsy. The hand, foot and ringworms are intermittent limbs (the most significant of the upper limbs), and the tendon is a "midwife" hand.
Cause
Cause
(1) Causes of the disease
The cause can be summarized as the following four categories:
1. Intracranial disease causes convulsions and convulsions
(1) Congenital diseases of the brain: such as brain penetrating malformation, microcephaly, hydrocephalus, fetal infection, various hereditary metabolic diseases, as well as maternal toxicity and radiation exposure during pregnancy, and acquired developmental defects.
(2) craniocerebral trauma: craniocerebral trauma is the most common cause of neonatal or infancy convulsions. The incidence of convulsions in adults with closed head trauma is 0.5% to 5%, and that of open injuries is 20% to 50%. The vast majority of cases occurred within 2 years after trauma.
(3) Brain infection: various encephalitis, meningitis, brain abscess and brain parasitic diseases.
(4) cerebrovascular disease: cerebral vascular malformation, subarachnoid hemorrhage, cerebral embolism, cerebral arteriosclerosis, cerebral thrombosis, intracranial venous sinus and venous thrombosis.
(5) intracranial tumors: common in the supratentorial tumor, especially oligodendroglioma (more than 60%), followed by meningioma and astrocytoma. Various metastases can also cause convulsions.
(6) Degenerative diseases of the brain: such as tuberous sclerosis, Alzheimer's disease, and Pick disease.
(7) Central demyelinating diseases: such as Schilder disease, multiple sclerosis, acute disseminated encephalomyelitis and the like.
2. Extracranial diseases lead to convulsions and convulsions
(1) cerebral hypoxia: such as asphyxia, shock, acute hemorrhage, carbon monoxide poisoning, inhalation anesthesia, etc.
(2) Metabolic endocrine diseases:
1 Amino acid metabolism abnormalities, such as phenylketonuria.
2 lipid metabolism disorders, such as lipid accumulation.
3 sugar metabolism diseases, such as hypoglycemia, galactosemia.
4 water, electrolyte disorders, such as hyponatremia, hypernatremia, water poisoning, hypokalemia, hypomagnesemia, hypercapnia and so on.
5 vitamin D deficiency, hypoparathyroidism.
6 vitamin deficiency and dependence, such as vitamin B6, vitamin B12 and folic acid deficiency.
(3) Poisoning:
1 drugs: such as central stimulant (nicaramide, pentylenetetrazol, camphor) excess; antipsychotic drugs (chlorpromazine, trifluoperazine, cloprofen, etc.) dose is too large; sudden withdrawal of anticonvulsant Or central nervous system inhibitors.
2 heavy metal poisoning, such as lead, mercury poisoning.
3 food, pesticide poisoning and alcohol withdrawal.
(4) Cardiovascular diseases: such as Adams-Stokes syndrome, hypertensive encephalopathy.
(5) Allergic or allergic diseases: such as penicillin and procaine allergies may become the cause.
3. Neurosis: snoring convulsions.
4. High fever: It is often the main cause of convulsions in infants and young children.
(two) pathogenesis
The mechanism of convulsions is extremely complex, and it can be a central nervous system function or structural abnormality, or it can be an abnormality of the peripheral nerve or even an effector, or both. According to the source of the abnormal electrical excitation signal, it can be divided into two cases:
1. Physiological and structural abnormalities of the brain: Under normal circumstances, well-developed brain neurons have a certain self-stabilizing effect, and their excitation and inhibition systems are in a relatively balanced state. Many brain or systemic diseases disrupt this balance, leading to decreased neuronal excitation thresholds and excessively synchronized discharges, thus causing convulsions.
(1) Decreased neuronal excitation threshold: The membrane potential of neurons is stable depending on the polarity distribution and structural integrity of the ions inside and outside the membrane. Many diseases inside and outside the brain can affect the stability of membrane potential through different ways. For example, hyponatremia and hyperkalemia directly cause a decrease in membrane potential (a decrease in neuronal excitation threshold), and the neurons are automatically depolarized to generate action potentials; Blood, hypoxia, hypoglycemia, hypomagnesemia and digitalis poisoning affect energy metabolism, or high heat causes excessive consumption of oxygen, glucose, and adenosine triphosphate, which can lead to a decrease in membrane potential; in addition, brain infection or extracranial infection The toxin directly damages the neuron membrane and increases its permeability. The low blood calcium causes the cells to increase the permeability of sodium ions, which can cause the extracellular sodium to flow in and cause the neurons to be automatically depolarized.
(2) Impaired brain neurons and their surrounding structures: various brain organic diseases (such as hemorrhage, tumor, contusion, encephalitis, brain abscess, etc.) can lead to sparse neurons, impaired membrane structure, and tree mutations. The shape, glial cell proliferation and astrocyte dysfunction lead to the loss of potassium ions, making it difficult for the neuron membrane to maintain a relatively stable polarization state, and it is easy to form spontaneous and long-term potential fluctuations.
(3) Neurotransmitter changes: When there are too many excitatory neurotransmitters, such as organophosphate poisoning, cholinesterase activity is inhibited, and excitatory transmitter acetylcholine accumulates too much, and convulsions can occur. Conversely, if the inhibitory neurotransmitter is too small, such as vitamin B6 deficiency, the lack of coenzyme of glutamate decarboxylase affects the conversion of glutamic acid decarboxylation to the production of the inhibitory transmitter -aminobutyric acid; Because glutamate is required for detoxification of ammonia by brain tissue, the precursor glutamate which is synthesized by -aminobutyric acid is reduced, and the result is convulsion.
(4) Mental factors: trauma can cause temporary dysfunction of cerebral cortex function, loss of regulation and inhibition of the subcortical center, leading to convulsions. Such as snoring convulsions.
(5) genetic factors: febrile seizures and idiopathic epilepsy have significant family aggregation, which suggests that genetic factors play a role in the occurrence of seizures, that is, the hereditary neuron excitability is reduced.
2. Non-brain dysfunction: mainly the movement of the spinal cord or peripheral nerves. For example, tetanus bacillus exotoxin selectively acts on synapses in the central nervous system (mainly the lower motor neurons of the spinal cord and brainstem), resulting in persistent myotonic convulsions. The poisoning of strychnine caused excessive excitability of the anterior horn cells of the spinal cord, which occurred like a tetanus-like convulsion.
In addition to increasing the permeability of neuronal membranes, hypocalcemia or alkalosis often exacerbates the excitability of peripheral nerves and sarcolemma by increasing the permeability of sodium ions, causing hand and foot spasms. In addition, tumors in the posterior cranial fossa, cerebellum, etc. or cerebellar tonsils affect brainstem function, and intermittent cortical rigidity may occur.
Examine
an examination
Related inspection
Brain Doppler ultrasound (TCD) EEG examination of brain CT examination ECG chest B-ultrasound
Select laboratory tests based on clues provided by medical history and physical examination. In addition to routine hematuria, blood biochemistry (blood sugar, electrolytes, etc.), blood gas analysis, heart, liver, kidney function tests and endocrine tests. Conventional, biochemical, and cytological examinations of cerebrospinal fluid contribute to the etiological diagnosis of central infection with convulsions.
1. Internal medicine: When the clinical suggestion that convulsions are caused by systemic diseases, the corresponding examination should be selected according to the clues provided. Including toxicology analysis, electrocardiogram, echocardiography, B-ultrasound and so on.
2. Nervous system: Once the neurological disease is suspected, the corresponding examination should be selected according to the location and nature of the disease.
Suspected epileptic seizures, EEG, SPECT scan and PET scan can be selected. Intracranial space-occupying lesions can be located and diagnosed by X-ray, brain CT and MRI. Cerebrovascular disease can be selected as cerebrovascular function tester, transcranial Doppler and angiography (qi brain, ventricle, brain) Angiography. The spinal cord or peripheral nerve with twitching can be diagnosed by electromyography and vertebral angiography.
Somatosensory evoked potentials and brainstem evoked potentials (auditory and visual evoked potentials) are important for the localization diagnosis of brain, spinal cord or peripheral nerves and muscle lesions.
Diagnosis
Differential diagnosis
The type of convulsions varies depending on the cause and the form of convulsions is different.
(1) systemic convulsions: for the body skeletal muscle contraction, such as epileptic seizures manifested as tonic-clonic convulsions; tetanus is continuous tonic convulsions.
(2) Localized convulsions: twitching the continuity of a part of the body or face. For example, localized sports epilepsy often manifests as repeated convulsions of the mouth, eyelids, hands or feet; if the convulsion starts from one place, it gradually expands according to the arrangement of the cerebral cortex movement area, that is, from the side of the thumb, the extension and the wrist , arms, shoulders, is Jackson epilepsy. The hand, foot and ringworms are intermittent limbs (the most significant of the upper limbs), and the tendon is a "midwife" hand.
Select laboratory tests based on clues provided by medical history and physical examination. In addition to routine hematuria, blood biochemistry (blood sugar, electrolytes, etc.), blood gas analysis, heart, liver, kidney function tests and endocrine tests. Conventional, biochemical, and cytological examinations of cerebrospinal fluid contribute to the etiological diagnosis of central infection with convulsions.
